Open access publications in the SLU publication database

Abstract

The transition to flowering in the facultative long-day plant Arabidopsis (Arabidopsis thaliana) have been thoroughly studied and today it is well understood how flowering in response to changes in photoperiod and cold is integrated at the molecular level. However it is less known how flowering is initiated in response to internal factors in the absence of environmental stimuli. Previously it have been shown that flowering under non inductive short-day conditions is dependent on the plant hormone gibberellin (GA). In an effort to improve the understanding on how GA promotes flowering we have analysed, which of the many GA’s that are florally active, and quantified the developmental changes of florally active GA’s in relation to floral initiation under short-day conditions. We found that GA4 had the highest floral activity and that presiding floral initiation there was a dramatic increase at the shoot apex in the content of GA4. Intriguingly we found that the expression of the rate limiting GA 20-oxidase remained stable at the time when GA started to increase, indicating that increased accumulation of GA in not caused by local production. With the help of knockout lines we show that removal of either GA20ox1 or GA20ox2 delayed flowering and hence that both genes is participating in the production of GA relevant for the transition to flowering. Analysis of the flowering behaviour of GA2ox mutants revealed that some ga2ox mutants flowered earlier. Reporter gene analysis showed that expression of the GA2ox gene which had highest impact on flowering time was localised to the shoot apex, indicating that the function of the GA 2-oxidase is to control accumulation of GA’s in the shoot apex. Analysis of the effect of late flowering mutations on flowering time in plants with increased GA signal transduction showed that the LD pathway functions mostly in parallel to GA’s and that late flowering in autonomous mutants is partially due to decreased GA signal transduction or decreased GA synthetic capacity.